title: Decreased production of human leukocyte antigen G molecules in sinonasal polyposis.
abstract: BACKGROUND
  Sinonasal polyposis (SNP) is a chronic inflammatory pathology of nasal and paranasal cavities. Human leukocyte antigen (HLA) G molecules are nonclassic class I antigens with anti-inflammatory and tolerogenic properties. As most theories consider polyps to be the manifestation of chronic inflammation, there could be a possible implication of HLA-G molecules in SNP. The purpose of this study was to investigate the possible correlation between SNP and the production of soluble HLA-G (sHLA-G) by peripheral blood mononuclear cells (PBMCs).
  
  
  METHODS
  The study involved 22 SNP patients (11 with no evidence of disease [NED] after surgery and 11 with relapse [RE]) and 20 healthy subjects. The presence of sHLA-G in PBMC lipopolysaccharide (LPS)-stimulated culture supernatants was analyzed. The levels of interleukin (IL) 10, one of the main up-regulators of sHLA-G production, were determined. Exogenous IL-10 was added to the SNP PBMC cultures to reconstitute the impairment in sHLA-G production.
  
  
  RESULTS
  Increased IL-10 levels in LPS-activated PBMC culture supernatants were found in NED patients in comparison with healthy subjects (p = 0.0184). No sHLA-G production was observed in either of the patient subgroup supernatants (p < 0.0001). The addition of exogenous IL-10 showed the reconstitution of sHLA-G production in NED and in a lower amount in RE patients.
  
  
  CONCLUSIONS
  The results show a defect in sHLA-G production in SNP patients mainly related to the IL-10/HLA-G pathway. Given the anti-inflammatory functions of HLA-G molecules, this impairment could increase the susceptibility to the disease. The different sHLA-G production after exogenous IL-10 addition between NED and RE SNP could represent a marker of disease severity.
authors.affiliation: Department of Ear, Nose, and Throat, University of Ferrara, Ferrara, Italy.
authors.forename: Nicola
authors.initials: N
authors.lastname: Malagutti
authors.forename: Claudia
authors.initials: C
authors.lastname: Aimoni
authors.forename: Alessandra
authors.initials: A
authors.lastname: Balboni
authors.forename: Marina
authors.initials: M
authors.lastname: Stignani
authors.forename: Loredana
authors.initials: L
authors.lastname: Melchiorri
authors.forename: Michela
authors.initials: M
authors.lastname: Borin
authors.forename: Antonio
authors.initials: A
authors.lastname: Pastore
authors.forename: Roberta
authors.initials: R
authors.lastname: Rizzo
authors.forename: Olavio Roberto
authors.initials: OR
authors.lastname: Baricordi
mesh_terms: D002478:Cells, Cultured; D005260:Female; D005434:Flow Cytometry; D005500:Follow-Up Studies; D006680:HLA Antigens / Q000096:biosynthesis* / Q000276:immunology; D059951:HLA-G Antigens; D015395:Histocompatibility Antigens Class I / Q000096:biosynthesis* / Q000276:immunology; D006801:Humans; D007118:Immunoassay; D016753:Interleukin-10 / Q000096:biosynthesis; D007963:Leukocytes, Mononuclear / Q000378:metabolism / Q000473:pathology; D008297:Male; D008875:Middle Aged; D009298:Nasal Polyps / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D010254:Paranasal Sinus Diseases / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D012189:Retrospective Studies; D012720:Severity of Illness Index
chemical_list: D006680:HLA Antigens; D059951:HLA-G Antigens; D015395:Histocompatibility Antigens Class I; D016753:Interleukin-10